CCNE1 amplification is associated with liver metastasis in gastric carcinoma

Kim, Binnari; Shin, Hyeong Chan; Heo, You Jeong; Ha, Sang Yun; Jang, Kee–Taek; Kim, Seung Tae; Kang, Won Ki; Lee, Jeeyun

doi:10.1016/j.prp.2019.152434

Cited by 23 publications

(17 citation statements)

References 20 publications

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“…Amplification of CCNE1 is associated with many cancer progressions including gastric cancer, bladder cancer, ovarian cancer and triple negative breast cancer and linked to poor prognosis. [40][41][42][43] In this study, we found that CCNE1 is up-regulated in cervical cancer cells. Functional studies showed that CCNE1 play critical roles in cervical cancer cell growth and cell cycle transition from G1to S phase.…”

Section: Discussionsupporting

confidence: 50%

“…Within the cell, CCNE1 forms a complex with and regulates the activity of CDK2, which further promotes cell cycle G1/S transition. Amplification of CCNE1 is associated with many cancer progressions including gastric cancer, bladder cancer, ovarian cancer and triple negative breast cancer and linked to poor prognosis 40‐43 . In this study, we found that CCNE1 is up‐regulated in cervical cancer cells.…”

Section: Discussionmentioning

confidence: 54%

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E6 hijacks KDM5C/lnc_000231/miR‐497‐5p/CCNE1 axis to promote cervical cancer progression

Zhang

et al. 2020

J Cellular Molecular Medi

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The prevalence of cervical cancer poses great threat to women's health. 1 Annually, over 500 000 patients were diagnosed with cervical cancer and approximately 300 000 died from this disease. 2-4 Due to the widely use of papanicolaou test for early cervical cancer screening and the advancement of therapeutic methods such as surgery operation, chemical treatment and radiotherapy, the incidence of cervical cancer has been reduced by 40%-50% in recent years. 5-7 However, for those advanced cervical cancer patients, the 5-year survival rate at the late stages can be as low as 15%. 8,9 Therefore, understanding the molecular mechanisms that initiate cervical cancer development and identifying new diagnostic markers are urgent for cervical cancer treatment, especially for those advanced cervical cancer patients. Nearly, all cervical cancer cases are linked to human papillomavirus (HPV) infection. Human papillomavirus is a small DNA tumour virus, consisting of a circular DNA molecule enclosed with capsid proteins. 10 Among all the genes encoded by HPV, E6 and E7 act as key oncogenes that promote tumour growth and malignant transformation. 11-14 Constitutive expression of E6/E7 immortalizes primary epithelial cells and promotes tumour formation in vivo. 15 E7 interacts with and stabilizes retinoblastoma tumour suppressor family (RB1 and RB2), facilitating cell cycle transition from G1 to S phase. 16 Similar to cell growth dysregulation, E6 interacting with ubiquitin ligase E6AP promotes tumour suppressor P53 degradation and cell proliferation. 17 Despite HPV infection, other cofactors also contribute to cervical cancer progression, such as immunosuppression, smoking, co-infection with HIV, co-infection with Chlamydia trachomatis and herpes simplex virus type 2 and other probable cofactors. 12

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Section: Discussionsupporting

confidence: 50%

Section: Discussionmentioning

confidence: 54%

E6 hijacks KDM5C/lnc_000231/miR‐497‐5p/CCNE1 axis to promote cervical cancer progression

Zhang

et al. 2020

J Cellular Molecular Medi

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“…CCNE1 (cyclin E1) mRNAs are significantly higher in GC tissues than in normal tissues in both Oncomine and The Cancer Genome Atlas (TCGA) datasets (Zhang et al, 2018) and this was also confirmed by the multiplex ligation-dependent probe amplification and fluorescence in situ hybridization (Ooi et al, 2017). Besides, it was also revealed that upregulated Cyclin E1 is highly associated gastric cancer development (Gu et al, 2010) and liver metastasis (Chang et al, 2009;Kim et al, 2019). In our study, qRT-PCR experiments showed that BD treatment could significantly reduce the expression of Cyclin E1, while overexpression of LINC01667 could restore the expression of Cyclin E1 to some extent.…”

Section: Discussionmentioning

confidence: 76%

Bruceine D inhibits Cell Proliferation Through Downregulating LINC01667/MicroRNA-138-5p/Cyclin E1 Axis in Gastric Cancer

Dong

Shi

et al. 2020

Front. Pharmacol.

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Objective: Gastric cancer is one of the most common malignant tumors. Bruceine D (BD) is one of the extracts of Brucea javanica. In recent years, it has been reported that BD has anti-tumor activity in some human cancers through different mechanisms. Here, this study try to explore the effect of BD on gastric cancer and its regulatory mechanism.Methods: Cell proliferation ability was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assays, 5-bromo-2-deoxyuridine (BrdU) staining and soft agar colony formation assay, respectively. The tumor xenograft model was used to verify the effect of BD on the tumorigenicity of gastric cancer cells in vivo. Flow cytometry analysis and Western blot assay were performed to detect cell cycle and apoptosis. Gastric cancer cells were analyzed by transcriptome sequencing. The interaction between LINC01667, microRNA-138-5p (miR-138-5p) and Cyclin E1 was verified by dual luciferase experiment and RT-PCR assays.Results: We found that BD significantly inhibited cell proliferation and induced cell cycle arrest at S phase in gastric cancer cells. Transcriptome analysis found that the expression of a long non-coding RNA, LINC01667, were significantly down-regulated after BD treatment. Mechanically, it was discovered that LINC01667 upregulated the expression of Cyclin E1 by sponging miR-138-5p. Furthermore, BD enhanced the chemosensitivity of gastric cancer cells to doxorubicin, a clinically used anti-cancer agent.Conclusion: BD inhibit the growth of gastric cancer cells by downregulating the LINC01667/miR-138-5p/Cyclin E1 axis. In addition, BD enhances the chemosensitivity of gastric cancer cells to doxorubicin. This study indicates that BD may be used as a candidate drug for the treatment of patients with gastric cancer.

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“…Our KEGG pathway annotation analysis showed that some pathways were closely related to liver cancer [ 53 ]. The cyclin dependent kinase CDK2 is the target of tumor treatment [ 54 ].…”

Section: Discussionmentioning

confidence: 99%

Uncovering the Mechanism of the Effects of Pien-Tze-Huang on Liver Cancer Using Network Pharmacology and Molecular Docking

Liu

Wang

Lou

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Pien-Tze-Huang (PTH) has a long history in the treatment of liver cancer. However, its molecular mechanism of action remains unclear. TCMSP and TCM were used to collect the active ingredients. Bioactive compounds targets were predicted by reverse pharmacophore models. The antiliver cancer targets of PTH were selected by gene comparison of liver cancer in the GEO database. Molecular docking was used to verify the binding activity of the targets and the active ingredients. The DAVID was used to analyze the gene function and signal pathway. A model was built with Cytoscape. The core genes were obtained by PPI network. We screened the 4 main medicinal ingredients of PTH to obtain 16 active ingredient, 190 potential targets, and 6 core genes. We found that active small molecules exert anticancer effects by multiple pathways. The core genes were involved in multiple biological processes. We also found that eight chemical components play a greater role in inhibiting liver cancer. PTH achieves the effect of inhibiting liver cancer through the synergistic effect of multiple components, multiple targets, and multiple pathways. This study provides a potential scientific basis for further elucidating the molecular mechanism of action of PTH against liver cancer.

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CCNE1 amplification is associated with liver metastasis in gastric carcinoma

Cited by 23 publications

References 20 publications

E6 hijacks KDM5C/lnc_000231/miR‐497‐5p/CCNE1 axis to promote cervical cancer progression

E6 hijacks KDM5C/lnc_000231/miR‐497‐5p/CCNE1 axis to promote cervical cancer progression

Bruceine D inhibits Cell Proliferation Through Downregulating LINC01667/MicroRNA-138-5p/Cyclin E1 Axis in Gastric Cancer

Uncovering the Mechanism of the Effects of Pien-Tze-Huang on Liver Cancer Using Network Pharmacology and Molecular Docking

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